title: Mast cell-associated alveolar inflammation in patients with atopic uncontrolled asthma.
abstract: BACKGROUND
  A significant proportion of patients with asthma have persistent symptoms despite treatment with inhaled glucocorticosteroids.
  
  
  OBJECTIVE
  We hypothesized that in these patients, the alveolar parenchyma is subjected to mast cell-associated alterations.
  
  
  METHODS
  Bronchial and transbronchial biopsies from healthy controls (n = 8), patients with allergic rhinitis (n = 8), and patients with atopic uncontrolled asthma (symptoms despite treatment with inhaled glucocorticosteroids; mean dose, 743 μg/d; n = 14) were processed for immunohistochemical identification of mast cell subtypes and mast cell expression of FcεRI and surface-bound IgE.
  
  
  RESULTS
  Whereas no difference in density of total bronchial mast cells was observed between patients with asthma and healthy controls, the total alveolar mast cell density was increased in the patients with asthma (P < .01). Division into mast cell subtypes revealed that in bronchi of patients with asthma, tryptase positive mast cells (MC(T)) numbers decreased compared with controls (P ≤ .05), whereas tryptase and chymase positive mast cells (MC(TC)) increased (P ≤ .05). In the alveolar parenchyma from patients with asthma, an increased density was found for both MC(T) (P ≤ .05) and MC(TC) (P ≤ .05). The increased alveolar mast cell densities were paralleled by an increased mast cell expression of FcεRI (P < .001) compared with the controls. The patients with asthma also had increased numbers (P < .001) and proportions (P < .001) of alveolar mast cells with surface-bound IgE. Similar increases in densities, FcεRI expression, and surface-bound IgE were not seen in separate explorations of alveolar mast cells in patients with allergic rhinitis.
  
  
  CONCLUSIONS
  Our data suggest that patients with atopic uncontrolled asthma have an increased parenchymal infiltration of MC(T) and MC(TC) populations with increased expression of FcεRI and surface-bound IgE compared with atopic and nonatopic controls.
authors.affiliation: Department of Respiratory Medicine and Allergology, Lund University, Lund, Sweden.
authors.forename: Cecilia K
authors.initials: CK
authors.lastname: Andersson
authors.forename: Anders
authors.initials: A
authors.lastname: Bergqvist
authors.forename: Michiko
authors.initials: M
authors.lastname: Mori
authors.forename: Thais
authors.initials: T
authors.lastname: Mauad
authors.forename: Leif
authors.initials: L
authors.lastname: Bjermer
authors.forename: Jonas S
authors.initials: JS
authors.lastname: Erjefält
mesh_terms: D000328:Adult; D001249:Asthma / Q000276:immunology*; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology*; D007073:Immunoglobulin E / Q000276:immunology; D007150:Immunohistochemistry; D007249:Inflammation / Q000276:immunology* / Q000473:pathology; D008297:Male; D008407:Mast Cells / Q000276:immunology*; D008875:Middle Aged; D011650:Pulmonary Alveoli / Q000276:immunology* / Q000473:pathology; D017455:Receptors, IgE / Q000276:immunology; D055815:Young Adult
chemical_list: D017455:Receptors, IgE; D007073:Immunoglobulin E